It is possible that important future biotechnologies to enhance human longevity might be built on top of a better understanding of the mechanisms that cause similarly sized species to have quite radically different life spans. It seems just as plausible as the idea of generating a family of age-slowing biotechnologies from a better understanding of human metabolism, though who is to say at this early stage in the game just how effective any final result might be. Still, research groups are successfully raising funds, sequencing genomes, and delving much deeper into the comparative biology of aging than has been the case in the past. For example:
As a group, birds are long-living with their maximum lifespan potential (MLSP) being on average twice that of similar-sized mammals, and it can be much greater for some individual comparisons. The most common mammal-bird comparison in the scientific literature is the rat-pigeon comparison. The rat has a MLSP of 5 y, compared to 35 y for the similar-sized pigeon (both from the AnAge database: genomics.senescence.info). This seven-fold MLSP difference has the potential to give considerable insight into the processes that determine longevity. Importantly, this is many times the longevity difference generally achieved either by genetic manipulation or environmental manipulation (such as dietary restriction).
We have revisited the rat-pigeon comparison in the most comprehensive manner to date. We have measured superoxide production (by heart, skeletal muscle and liver mitochondria), five different antioxidants in plasma, three tissues and mitochondria, membrane fatty acid composition (in seven tissues and three mitochondria), and biomarkers of oxidative damage. The only substantial and consistent difference that we have observed between rats and pigeons is their membrane fatty acid composition, with rats having membranes that are more susceptible to damage.
That's a pretty good piece of supporting evidence for the membrane pacemaker hypothesis of aging: longer lived species are longer lived because their cellular membranes are more resistant to damage. This ties in nicely to the role of mitochondria and mitochondrial damage in aging: swarming mitochondria in cells churn out damaging free radicals as a consequence of their day to day operations, and as a consequence damage themselves in ways that spiral out to cause all sorts of harm in the long term. If a species is more resistant to that damage in the places where it matters the most, then it lives longer.
As I have said before, I tend to view this as support for the importance of mitochondrial repair research. If resistant mitochondria give pigeons even a fair chunk of that multiplier of seven over rat life spans, then how much further could the research community take things if armed with a way to completely fix the self-inflicted mitochondrial damage rather than just resist it?